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Article

BRAF inhibitor resistance enhances vulnerability to arginine deprivation in melanoma.

Oncotarget - 5 Apr 2016

Li Ying-Ying, Wu Chunjing, Chen Shu-Mei, Shah Sumedh S, Wangpaichitr Medhi, Feun Lynn G, Kuo Macus T, Suarez Miguel, Prince Jeffrey, Savaraj Niramol

Abstract excerpt

BRAF inhibitor (BRAFi) has been used for treatment of melanomas harboring V600E mutation. Despite a high initial response rate, resistance to BRAFi is inevitable. Here, we demonstrate that BRAFi-resistant (BR) melanomas are susceptible to arginine deprivation due to inability to initiate re-expression of argininosuccinate synthetase (ASS1, a key enzyme for arginine synthesis) as well as ineffective autophagy....

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Share to Arginine
Share to Autophagy

Methodology Data sources Editorial policy Privacy About Contact Helena Bioinformatics

Share to Drug Resistance, Neoplasm

Share to Melanoma

Share to Mice, Nude

Share to Protein Kinase Inhibitors

Share to Proto-Oncogene Proteins B-raf

Share to Xenograft Model Antitumor Assays

Source

Open in PubMed Open full text

Identifiers

PMID: 26771234
DOI: 10.18632/oncotarget.6882
PMCID: PMC4951241

Genes

ASS1
BRAF
USP28

Variants

Provenance

PubMed metadata and Literature Corpus relationships. Corpus snapshot updated 7 Sept 2026. Manifest publication-graph-cohort-2026-09-07.1.

Source receipt: pubmed, retrieved 7 Sept 2026.

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